Liver fibrosis

By M. Pinzani. Springer Seminars in Immunopathology, 2004

2,559 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology

View Paper: https://www.semanticscholar.org/paper/ad997eec89454e682d08f7141c2a861adc46ea32

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. F. Tacke
2. S. Friedman
3. M. Pinzani
4. Ralf Weiskirchen
5. D. Brenner
6. TA Wynn
7. A. Gressner
8. Luke Barron

In Hepatology

1. S. Friedman
2. F. Tacke
3. Ralf Weiskirchen
4. D. Brenner
5. M. Pinzani
6. A. Gressner
7. TA Wynn
8. Luke Barron

Citations in the corpus

• Elastography for the diagnosis of severity of fibrosis in chronic liver disease: a meta-analysis of diagnostic accuracy. (2011, background): “This is important, as comparing the two techniques at a similar point minimises differences due to progression of fibrosis, which may not be constant over time [1].”
• Macrophages: Master Regulators of Inflammation and Fibrosis (2010, background): “In the liver, TGF-b1 promotes fibrosis by prompting HSC differentiation into myofibroblasts, enhancing expression of tissue inhibitors of matrix metalloproteases (TIMPs) that block ECM degradation, and by directly promoting synthesis of interstitial fibrillar collagens.(1) PDGF also acts as a potent”
• The Hippo signalling pathway and its implications in human health and diseases (2022, background): “Hepatic fibrosis results from chronic liver damage, which can be caused by NASH, alcohol abuse or hepatitis virus infection.(335) Carbon tetrachloride (CCl4) is a hepatotoxin that is widely used to establish hepatic fibrosis animal models.”
• Myofibroblasts revert to an inactive phenotype during regression of liver fibrosis (2012, methodology): “, hepatitis B virus, hepatitis C virus, biliary obstruction, or alcohol) and in rodents [carbon tetrachloride (CCl4) or bile-duct ligation] produces regression of liver fibrosis and is associated with decreased cytokine and ECM production, increased collagenase activity, and the disappearance of myo”
• Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-β as major players and therapeutic targets (2006, background): “Formal pathogenesis of fibrosis is initiated by parenchymal cell destruction (necrosis rather than apoptosis) due to multiple injurious agents and mechanisms followed by inflammation, which in turn activates “resting” hepatic stellate cells (HSC), formerly called fat or vitamin A or retinoid storing”
• EMT and tumor metastasis (2015, background): “Cirrhosis can lead to the activation of stellate cells, which increase production of extracellular matrix proteins, cytokines, and growth factors, many of which can alter hepatocyte proliferation and promote tumorigenesis [93,94].”
• Pathogenesis of non-alcoholic fatty liver disease (2009, background): “Indeed, the creation of a progenitor cell niche, with deposition of matrix, may act not only as a migratory pathway for HPCs to migrate along from the portal tract into the parenchyma, but also provide trophic factors for the survival of these cells.(103)”
• Hepatic fibrosis: Concept to treatment. (2015, background): “In contrast, chronic liver injury, as triggered by different etiologies, induces repetitive tissue damage, resulting in impaired regenerative capacity marked by an altered inflammatory infiltrate and a chronic wound healing response [1,2].”
• Elevated levels of von Willebrand Factor in cirrhosis support platelet adhesion despite reduced functional capacity (2006, background): “whereas in the reference group the median VWF propeptide level was 89% [30-237]) (P .”